2012
Y265C DNA polymerase beta knockin mice survive past birth and accumulate base excision repair intermediate substrates
Senejani AG, Dalal S, Liu Y, Nottoli TP, McGrath JM, Clairmont CS, Sweasy JB. Y265C DNA polymerase beta knockin mice survive past birth and accumulate base excision repair intermediate substrates. Proceedings Of The National Academy Of Sciences Of The United States Of America 2012, 109: 6632-6637. PMID: 22493258, PMCID: PMC3340078, DOI: 10.1073/pnas.1200800109.Peer-Reviewed Original ResearchConceptsDNA polymerase activityWT littermatesKnockin miceMiceMouse embryo fibroblastsChromosomal aberrationsWT mouse embryo fibroblastsNormal Mendelian ratioSlow proliferationPolymerase activityBirthΒ variantCell deathEmbryo fibroblastsWT cellsExcision repair pathwayDNA repair systemsCellular metabolismBase excision repair pathwayFibroblastsHoursHigh levelsHomozygous mutantsKey players
2008
Separating Genetic and Hemodynamics Effects In Nrp1 Knockout Embryos
Jones E, Yuan L, Breant C, Watts R, Eichmann A. Separating Genetic and Hemodynamics Effects In Nrp1 Knockout Embryos. The FASEB Journal 2008, 22: 1143.2-1143.2. DOI: 10.1096/fasebj.22.1_supplement.1143.2.Peer-Reviewed Original Research
2004
Disruption of neural signal transducer and activator of transcription 3 causes obesity, diabetes, infertility, and thermal dysregulation
Gao Q, Wolfgang MJ, Neschen S, Morino K, Horvath TL, Shulman GI, Fu XY. Disruption of neural signal transducer and activator of transcription 3 causes obesity, diabetes, infertility, and thermal dysregulation. Proceedings Of The National Academy Of Sciences Of The United States Of America 2004, 101: 4661-4666. PMID: 15070774, PMCID: PMC384803, DOI: 10.1073/pnas.0303992101.Peer-Reviewed Original ResearchMeSH KeywordsAcute-Phase ProteinsAdipose Tissue, BrownAnimalsBody Temperature RegulationCorticosteroneDiabetes MellitusDNA-Binding ProteinsFemaleInfertility, FemaleInfertility, MaleIntermediate Filament ProteinsKineticsLeptinMaleMiceMice, KnockoutMice, TransgenicNerve Tissue ProteinsNestinObesityRatsSTAT3 Transcription FactorTime FactorsTrans-ActivatorsConceptsSignal transducerActivator of transcriptionApparent developmental abnormalitiesEnergy homeostasisGenetic modelsTranscription 3Mendelian ratioHomozygous mutantsCold stressNeonatal lethalityPhysiological roleMutantsGlial differentiationUnique phenotypeSTAT3Essential roleDevelopmental abnormalitiesHomeostasisActivatorNeuroendocrine defectsTranscriptionDisruptionProteinKnockoutReproduction
2001
Two Splice Variants of the Wilms' Tumor 1 Gene Have Distinct Functions during Sex Determination and Nephron Formation
Hammes A, Guo J, Lutsch G, Leheste J, Landrock D, Ziegler U, Gubler M, Schedl A. Two Splice Variants of the Wilms' Tumor 1 Gene Have Distinct Functions during Sex Determination and Nephron Formation. Cell 2001, 106: 319-329. PMID: 11509181, DOI: 10.1016/s0092-8674(01)00453-6.Peer-Reviewed Original ResearchMeSH KeywordsActive Transport, Cell NucleusAlternative SplicingAnimalsAnimals, NewbornApoptosisBase SequenceCell SurvivalDAX-1 Orphan Nuclear ReceptorDisorders of Sex DevelopmentDNA-Binding ProteinsExonsFemaleGenes, Wilms TumorGlomerulosclerosis, Focal SegmentalGonadsMaleMiceMutagenesisNephronsNuclear ProteinsProtein IsoformsReceptors, Retinoic AcidRepressor ProteinsRNA Splice SitesRNA, MessengerSex Determination ProcessesSex-Determining Region Y ProteinSyndromeTranscription FactorsWT1 ProteinsConceptsTumor 1 geneDistinct functionsKTS isoformsSex determination pathwaySplice variantsDistinct molecular functionsZinc finger 3XY sex reversalWilms' tumor 1 geneMolecular functionsWT1 resultsAlternative splicingSex determinationSex reversalFinger 3Nephron formationHomozygous mutantsSpecific isoformsImportant regulatorExpression levelsIsoformsKidney defectsFrasier syndromeHeterozygous miceMouse strainsBcl-XL–Caspase-9 Interactions in the Developing Nervous System: Evidence for Multiple Death Pathways
Zaidi A, D'Sa-Eipper C, Brenner J, Kuida K, Zheng T, Flavell R, Rakic P, Roth K. Bcl-XL–Caspase-9 Interactions in the Developing Nervous System: Evidence for Multiple Death Pathways. Journal Of Neuroscience 2001, 21: 169-175. PMID: 11150333, PMCID: PMC6762421, DOI: 10.1523/jneurosci.21-01-00169.2001.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisbcl-2-Associated X Proteinbcl-X ProteinCaspase 3Caspase 9CaspasesCells, CulturedCytarabineGanglia, SpinalGenes, LethalHeterozygoteHomozygoteImmunohistochemistryIn Situ Nick-End LabelingLiverMiceMice, KnockoutNervous SystemNeuronsProto-Oncogene ProteinsProto-Oncogene Proteins c-bcl-2TelencephalonTumor Suppressor Protein p53ConceptsGene family membersCaspase-9 deficiencyCaspase-9Telencephalic neural precursor cellsCell deathDouble homozygous mutantsCaspase family membersMultiple death pathwaysNormal nervous system developmentBcl-2Nervous system developmentBax-deficient neuronsNeuronal apoptosisTelencephalic neuronsDeficient embryosNeural precursor cellsDeath pathwaysFamily membersHomozygous mutantsApoptotic pathwayObligate pathwayBcl-xLApoptosis inducersDeficient neuronsTargeted disruption
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